Transcription-coupled repair of 8-oxoguanine in human cells and its deficiency in some DNA repair diseases

被引：22

作者：

Gallego, MP ^{[1
]}

Sarasin, A ^{[1
]}

机构：

[1] Inst Gustave Roussy, CNRS, UPR 2169, Lab Genet Instabil & Canc, F-94805 Villejuif, France

来源：

BIOCHIMIE | 2003年 / 85卷 / 11期

关键词：

8-oxoguanine; transcription-coupled repair; RNA polymerase II; Cockayne syndrome; neurological disorders; ageing;

D O I：

10.1016/j.biochi.2003.11.005

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

8-Oxoguanine (8-oxoG) is a major oxidized base found in DNA due to endogenous or exogenous pro-oxidant agents. In the absence of repair, this lesion has a high mutation potency giving rise mainly to G:C to A:T transversions. 8-oxoG can be removed by the classical base excision repair pathway but can also be eliminated by a transcription-coupled repair (TCR) process that needs the wild type activities of CSB, XPG, XPB, XPD, BRCA1, BRCA2 and MSH2 proteins. The lack of TCR of oxidative lesions may lead to dramatic hereditary diseases like Cockayne syndrome. Accumulation of unrepaired oxidized bases in brain cells may explain the progressive neurological deterioration found in some DNA repair-deficient patients. (C) 2003 Elsevier SAS. All rights reserved.

引用

页码：1073 / 1082

页数：10

共 81 条

[41]

LIU J, 1995, MOL CELL BIOL, V15, P6729

[42] Recovery of RNA synthesis from the DHFR gene following UV-irradiation precedes the removal of photolesions from the transcribed strand [J].

Ljungman, M .

CARCINOGENESIS, 1999, 20 (03) :395-399

[43] Ultraviolet radiation alters the phosphorylation of RNA polymerase II large subunit and accelerates its proteasome-dependent degradation [J].

Luo, ZH ;

Zheng, JH ;

Lu, Y ;

Bregman, DB .

MUTATION RESEARCH-DNA REPAIR, 2001, 486 (04) :259-274

[44] UV light-induced degradation of RNA polymerase II is dependent on the Cockayne's syndrome A and B proteins but not p53 or MLH1 [J].

McKay, BC ;

Chen, F ;

Clarke, ST ;

Wiggin, HE ;

Harley, LM ;

Ljungman, M .

MUTATION RESEARCH-DNA REPAIR, 2001, 485 (02) :93-105

[45] Transcription-coupled repair deficiency and mutations in human mismatch repair genes [J].

Mellon, I ;

Rajpal, DK ;

Koi, M ;

Boland, CR ;

Champe, GN .

SCIENCE, 1996, 272 (5261) :557-560

[46] COCKAYNE SYNDROME - REVIEW OF 140 CASES [J].

NANCE, MA ;

BERRY, SA .

AMERICAN JOURNAL OF MEDICAL GENETICS, 1992, 42 (01) :68-84

[47] MSH2 and MSH6 are required for removal of adenine misincorporated opposite 8-oxo-guanine in S-cerevisiae [J].

Ni, TT ;

Marsischky, GT ;

Kolodner, RD .

MOLECULAR CELL, 1999, 4 (03) :439-444

[48] Expression and differential intracellular localization of two major forms of human 8-oxoguanine DNA glycosylase encoded by alternatively spliced OGG1 mRNAs [J].

Nishioka, K ;

Ohtsubo, T ;

Oda, H ;

Fujiwara, T ;

Kang, DC ;

Sugimachi, K ;

Nakabeppu, Y .

MOLECULAR BIOLOGY OF THE CELL, 1999, 10 (05) :1637-1652

[49]

Nunomura A, 1999, J NEUROSCI, V19, P1959

[50] A global DNA repair mechanism involving the Cockayne syndrome B (CSB) gene product can prevent the in vivo accumulation of endogenous, oxidative DNA base damage [J].

Osterod, M ;

Larsen, E ;

Le Page, F ;

Hengstler, JG ;

van der Horst, GT ;

Boiteux, S ;

Klungland, A ;

Epe, B .

ONCOGENE, 2002, 21 (54) :8232-8239

← 1 2 3 4 5 6 7 8 9 →